Ultraviolet B (UVB) irradiation induces both production of reactive oxygen species (ROS) and glucocorticoids (GCs)-mediated stress responses such as an increase of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity in skin. In addition, ROS-induced inflammatory mediators and proinflammatory cytokines trigger skin inflammation. In this study, as 11β-HSD1 inhibitor recovered a decrease of catalase expression, we investigated whether Trapa japonica (TJ) extract and its fractions could inhibit 11β-HSD1/ROS-induced skin inflammation in HaCaT keratinocytes. TJ extract and its fractions inhibited expressions of 11β-HSD1 as well as the increase of ROS in UVB-exposed HaCaT keratinocytes. Moreover, proinflammatory cytokines such as interleukin (IL)-α, -β and tumor necrosis factor (TNF)-α, and cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) as inflammatory mediators were also inhibited in both mRNA and protein levels. Finally, prostaglandin E 2 (PGE 2 ) produced by COX-2 was inhibited effectively by TJ extract and its fractions. Taken together, these results suggest that TJ extract could be a potential anti-inflammatory ingredient to inhibit UVB-induced inflammation in skin.

Ultraviolet B (UVB) is a primary environmental factor that induces adverse effects on skin such as photoaging, skin burn and cancer. UVB also increases the expression of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive cortisone to active cortisol in response to a variety of stressors in target tissues. Thus, we have screened new herbal extracts that suppress 11β-HSD1 expression induced by UVB in human dermal fibroblasts. We also investigated whether Trapa japonica (TJ) extract and its fractions inhibit UVB-induced photoaging in Hs68 cells and 3D skin model. Results showed that TJ extract inhibited the increase of 11β-HSD1 expression in UVB-exposed Hs68 cells significantly. TJ extract and its fractions not only inhibited 11β-HSD1 expression, but also suppressed the increase of matrix metalloproteinases 3,9) and proinflammatory cytokines 8) in UVB-irritated Hs68 cells. TJ extract also inhibited MMP-1 expression in UVB-irritated 3D skin model. In addition, TJ extract recovered UVB-induced decreases of epidermal thickness and PCNA-positive cells in 3D skin model. Taken together, these results suggest that TJ extract and its fractions inhibit UVB-induced skin photoaging by interfering with 11β-HSD1 and MMPs.

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